Theories of
biological aging need to explain how aging relates to the evolution process.
More specifically, if the evolution process has caused organisms to evolve
myriad other ways to survive longer and reproduce more, why does aging still
exist? As summarized below, aging theories propose three different answers to
this question and are based on three different versions of Darwin's survival of
the fittest idea.

Many people believe that
biological aging is simply the result of universal deteriorative processes such
as oxidation, entropy, or wear and tear that cause aging in machinery, exterior paint, and
other inanimate objects. These theories are superficially attractive if only
human aging is considered but fail if life span characteristics of other species
are also examined.

As we learn in biology class,
Darwin's "survival of the fittest" idea says that the evolution process causes
organisms to acquire inheritable design characteristics or traits that help
them survive longer and breed more. Deterioration and death from aging clearly
does not help humans to live longer and breed more so why do we age? Wouldn't
the evolution process have led to longer and longer lived animals eventually
resulting in immortality? Contemporaries actually wrote Darwin and asked this
question! The obvious answer is that aging results from fundamental limitations
such as laws of physics or chemistry that, by definition, cannot be overcome by
the evolution process.

There is no question but that
many aspects of aging look likethe accumulation of damage. Examples are
oxidative damage, mutations, and the protein cross-linkages that cause our
collagen to lose flexibility with age. But the essential mystery is why the
body is able to avoid these problems for many decades, but then permits the
damage to occur in old age. And why do some animals age so much more slowly
than other, very similar animals? Why would universal laws of physics or
chemistry affect biochemically very similar species so differently. (Mouse-sized naked mole rats live
~30 years, while mice
live ~2 years.) These are reasons that aging requires a more complex
explanation.

Consequently few bioscientists still believe
in simple deterioration or "accumulated damage" theories although deteriorative processes
such as oxidation and other molecular damage are part of most aging
theories. See longer description
of wear and tear theories.

Because they are a logical
consequence of Darwin's theory as widely taught, fundamental limitation theories
are still widely believed by the general science-aware public.

Medawar's Hypothesis
- Evolutionary Value of Survival Declines with Age

Peter Medawar, a famous and
eventually Nobel-prize-winning British zoologist, published a modification to
Darwin's theory in 1952 that
is important to all subsequent evolutionary theories of aging. He suggested that
the evolutionary need to live longer decreases following the age at which an organism is first capable of reproducing
and also depends on many other internal and external circumstances that are
specific to a particular species such as gestation time, mating seasons,
predation, and seasonal attrition. Although theorists
now disagree regarding details of Medawar's hypothesis
everybody agrees that an organism that died of old age prior to reaching puberty
would not make logical sense. There would therefore be strong evolutionary force
toward avoiding aging until the age at which an organism could complete a
first reproduction. Medawar further suggested that there would be
no evolutionary benefit from a species evolving ways to overcome
internal causes of deterioration (aging) beyond the age at which
essentially all of the individuals would have died from external
causes. If a thousand mice were born today we could easily imagine that under
wild conditions few would survive more than two years and therefore the internal
ability to survive longer would not have any evolutionary value. This hypothesis was widely embraced
by bioscientists because it provided a good explanation
for the gross variation in life spans seen in different, but biochemically
similar, species.

Medawar's idea was that under
wild conditions, aging did not cause any significant deleterious effect on a
species population. Immortality or even just a somewhat longer lifespan would
not help a population and therefore did not evolve.

Modern Non-Programmed
Aging Theories

Modern non-programmed aging theories are
based on Medawar's hypothesis, which
holds that organisms can and
do evolve myriad complex biological mechanisms directed at achieving a lifespan
at least able to complete a first reproduction and that the design of any
organism must support surviving for a particular minimum lifespan.

Multiple theorists including G.
Williams and T. Kirkwood subsequently attacked Medawar's idea by observing that aging did cause at
least some deleterious effect on wild mammal populations contrary to Medawar's
zero-disadvantage idea. Wild animal studies confirmed this by showing that wild
animal death rates increased with age, which presumably would not happen in an
immortal population, or one in which aging caused no disadvantage. These theorists therefore concluded that
aging must convey some compensating benefit to offset the declined
but still non-zero disadvantage of aging. Some non-programmed theories contend that aging is an unavoidable adverse side-effect of some beneficial
function. Because of Medawar's declining value hypothesis, a beneficial function that
contributed to an animal's early life in even a minor way could offset even
catastrophic disadvantage (e.g. death of old age) in later life. All such
theories have to explain why the evolution process was unable to find a way to
accomplish the beneficial effect without the adverse side-effect, a significant
difficulty and one of the problems with non-programmed theories.

Non-programmed theories compete
with each other, have apparent logical flaws, and have difficulty in explaining
many observations.

The following articles contain
descriptions of each of the main non-programmed
(non-adaptive, passive) theories of mammal aging including discussion of their apparent logical
flaws:

Developmental (DevAge) or
Life-history theories of aging contend that aging is an adverse side-effect of
the development or growth process. From an evolutionary viewpoint these are
versions of "aging is an unavoidable adverse side-effect of some beneficial function."

Population
Benefit Evolution Theories

Beginning in 1962 a series of new
modifications to Darwin's survival of the fittest idea appeared to the effect
that an organism trait that caused a long-term or population benefit such as
decreased probability that a species would become extinct could evolve even if
that trait caused some degree of short-term or individual disadvantage such as
reduced probability that an individual would produce adult descendants. There
are now multiple theories including group selection (benefit to a group can
offset individual disadvantage), kin selection (benefit to close relatives can
offset individual disadvantage), evolvability theory (traits that increase a
population's
ability to evolve can offset individual disadvantage), and gene-oriented
theories (traits that assist propagation of genes can offset individual
disadvantage).

Darwin's evolutionary concept
(random mutations occur, natural selection selects those that increase the possessing individual's ability to survive and reproduce) is
incompatible with the population benefit theories. However, in the intervening
150+ years enormous advances in our understanding of the biological inheritance
process have led to an understanding that the evolution process is actually much
more complex than suggested by Darwin. Some of the additional complexities
specifically favor the population benefit concepts and there is now an extensive
theoretical basis for the idea that the population benefit theories (maybe even
all of them) are valid. In addition to aging (see below) the population benefit
theories provide explanations for other observations that appear to conflict
with Darwin's ideas including animal altruism, sexual reproduction, some mating
rituals, and delayed puberty.

Programmed
Aging Theories

Programmed aging theories are
based on the idea that living too long creates an evolutionary
disadvantage and that therefore organisms evolved a suicide mechanism or
senescence program that purposely limits the lifespan of the
organism beyond a species-specific age. These theories are based on Medawar's
idea that the evolutionary benefit of survival declines with age and also the idea
that a limited lifespan creates benefit according to one of the population
benefit theories. Collectively, these theorists have suggested many ways in
which purposely limited lifespan creates population benefit. According to
programmed theories the compensating benefit of aging is a direct population
benefit instead of a side-effect of some individual benefit.

Programmed
theories fit observations better than non-programmed theories. These are
the
programmed aging theories listed by underlying population benefit theory:

Living organisms possess extensive maintenance and repair capabilities. These
capabilities are central to programmed and non-programmed Maintenance Theories of
Aging.

Programmed theories suggest that each organism has an optimum
lifespan determined by many internal and external species-specific
circumstances. Regulated programmed aging theories suggest
that an organism design having the ability to adjust (regulate) an individuals
lifespan in response to sensing local or temporary changes in internal or external conditions that affect
optimum lifespan such as famine, drought, or reproductive conditions would
provide an evolutionary benefit. Regulated mechanisms are common in biology and
regulation of lifespan in response to temporary conditions like famine or
drought matches observations like experiments showing that caloric restriction
increases lifespan.

Aging Theories and Medical
Research

Programmed and non-programmed
theories of aging lead to very different concepts regarding biological
mechanisms of aging, which in turn lead to very different approaches in
attempting to prevent and treat age-related diseases. In general, non-programmed
theories consider that each manifestation of aging is independent of the others
such that attempts to treat or prevent age-related diseases or conditions must
be separately devised and applied to each disease or condition. Aging, per se, is an
untreatable condition. Historically, the vast majority of medical research and
resulting treatments have
been based on this idea.

Programmed aging theories suggest
that the many different manifestations and conditions are ultimately controlled, at least
to some extent, by a suicide mechanism or program, and that therefore medical
efforts toward interfering with the program can generally delay aging.
Anti-aging medicine is therefore possible. Treatments directed at
specific disease mechanisms are still valid but programmed theories suggest additional ways in which diseases of aging could be attacked. Because
this is a substantially new approach, we could reasonably expect relatively
rapid progress.

There is no scientific agreement
regarding which of the many current versions of Darwin's survival of the fittest
idea is correct; nor is there any agreement regarding the dependent programmed
or non-programmed aging theories. Proponents of modern non-programmed theories
generally accept Medawar's modification of Darwin's theory but reject all of the
subsequent population benefit theories and associated programmed aging theories.

However, major investments are
now being made in research based on programmed aging theories: See Google Calico Research Company and NIH Interventions Testing
Program. The idea that aging is itself a treatable condition is
increasingly accepted. For example, the American Academy of Anti-Aging
Medicine claims 26,000 physician and researcher members.